Inhibitory effect of pentachlorophenol on gap junctional intercellular communication in rat liver epithelial cells in vitro

Sai, Kimie; Upham, Brad L.; Kang, Kyung-Sun; Hasegawa, Ryohei; Inoue, Takahiro; Trosko, J. E.

doi:10.1016/s0378-4274(98)80723-6

Cited by 6 publications

(10 citation statements)

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“…WB-F344 stem-like cell line used in our study have the characteristics of oval cells, which have been implicated as the target cell type in liver cancer (Sell, 1993; Ruch and Trosko, 1999) and their proliferation is often seen in the early stages of diseased states that lead to cancer not only in rodents but also humans (Roskams et al, 1998; Lowes et al, 1999). Also, the effects of cyanobacterial extracts on GJIC and ERK1/2 in WB-F344 cells are very similar to the effects of many well-recognized nongenotoxic carcinogens and tumor promoters such as phorbolesters (Madhukar et al, 1996), polycyclic aromatic hydrocarbons (Blaha et al, 2002), polychlorinated biphenyls, PCBs (Kang et al, 1996; Machala et al, 2003), organochlorine pesticides (Trosko et al, 1987; Upham et al, 1997; Sai et al, 1998; Masten et al, 2001), perfluorinated fatty acids (Upham et al, 1998a) or organic peroxides (Upham et al, 2007). Thus, our results suggest not only an existence of so far uncharacterized tumor promoting chemicals of cyanobacterial origin and an involvement of GJIC and MAPK activation in cyanobacteria-associated tumor promotion, but also a possible role of adult stem or stem-like cells in cyanobacteria-induced carcinogenesis.…”

Section: Discussionmentioning

confidence: 75%

Inhibition of gap-junctional intercellular communication and activation of mitogen-activated protein kinases by cyanobacterial extracts – Indications of novel tumor-promoting cyanotoxins?

Bláha

Babica

Hilscherová

et al. 2010

Toxicon

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Toxicity and liver tumor promotion of cyanotoxins microcystins have been extensively studied. However, recent studies document that other metabolites present in the complex cyanobacterial water blooms may also have adverse health effects. In this study we used rat liver epithelial stem-like cells (WB-F344) to examine the effects of cyanobacterial extracts on two established markers of tumor promotion, inhibition of gap-junctional intercellular communication (GJIC) and activation of mitogen-activated protein kinases (MAPKs) – ERK1/2. Extracts of cyanobacteria (laboratory cultures of Microcystis aeruginosa and Aphanizomenon flos-aquae and water blooms dominated by these species) inhibited GJIC and activated MAPKs in a dose-dependent manner (effective concentrations ranging 0.5 - 5 mg d.w./mL). Effects were independent of the microcystin content and the strongest responses were elicited by the extracts of Aphanizomenon sp. Neither pure microcystin-LR nor cylindrospermopsin inhibited GJIC or activated MAPKs. Modulations of GJIC and MAPKs appeared to be specific to cyanobacterial extracts since extracts from green alga Chlamydomonas reinhardtii, heterotrophic bacterium Klebsiella terrigena, and isolated bacterial lipopolysaccharides had no comparable effects. Our study provides the first evidence on the existence of unknown cyanobacterial toxic metabolites that affect in vitro biomarkers of tumor promotion, i.e. inhibition of GJIC and activation of MAPKs.

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Section: Discussionmentioning

confidence: 75%

Inhibition of gap-junctional intercellular communication and activation of mitogen-activated protein kinases by cyanobacterial extracts – Indications of novel tumor-promoting cyanotoxins?

Bláha

Babica

Hilscherová

et al. 2010

Toxicon

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“…TPA inhibits GJIC (gap junctional intercellular communication) in several kinds of cell lines including WB-F344 rat liver epithelial cells [175]. EC at the concentration of 27.8 lg/mL prevented the TPA-induced GJIC inhibition by about 60% [99].…”

Section: -O-tetradecanoylphorbol-13-acetatementioning

confidence: 98%

Green tea: protective action against oxidative damage induced by xenobiotics

Kaushik

Satya

Naik

2010

Mediterr J Nutr Metab

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The indiscriminate usage of synthetic chemicals and pesticides has led to a widespread contamination of land, water and air with harmful xenobiotics. The exposure to these toxicants results in severe health effects on organisms. Also, some natural foods contain harmless chemical species (nitrate), which however become toxic on certain conditions. Hence it is pertinent to focus attention on commonly consumed plant food materials, which can neutralize the toxicity damage caused by environmental agents. One of the most important sources of antioxidants is green tea. This review focuses on the mechanisms of oxidative damage caused by different xenobiotics and the defensive action of green tea in mitigating the damage. It is concluded that tea polyphenols, catechins and flavonoids scavenge reactive oxygen species and render a protective effect.

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“…Retinoids and carotenoids were the first dietary components shown to up-regulate GJIC (58,59). Green tea components, which have been shown to affect carcinogenesis (60), could prevent the down-regulation of tumor promoters, such as PCP, both in vitro and in vivo in rat liver (61,62). Kaempferol, a component of vegetables, could restore GJIC in human cancer cells (63).…”

Section: Role Of Gjic In Dietary Chemoprevention and Chemotherapymentioning

confidence: 99%

Dietary Modulation of the Multistage, Multimechanisms of Human Carcinogenesis: Effects on Initiated Stem Cells and Cell–Cell Communication

Trosko¹

2006

Nutrition and Cancer

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Diet can influence the risk to cancer in both negative and positive ways. Worldwide, more than 10 million persons develop cancer annually. Diet could prevent many cancers. Carcinogenesis is a multistage, multimechanism process, consisting of "initiation," "promotion," and "progression" phases. Although diet could affect each phase, an efficacious strategy for dietary chemoprevention would be intervention during the promotion phase. The tumor-promotion process requires sustained exposure to agents that stimulate the growth and inhibition of apoptosis of initiated cells in the absence of antipromoters. Chronic inflammation has been associated with the promotion process. The mechanism affecting the promotion process appears to be the inhibition of cell-cell communication between normal and initiated cells. Most, if not all, tumor-promoting agents and conditions, reversibly, inhibit cell-cell communication, whereas antipromoters, antioxidants, and anti-inflammatory agents have been shown to ameliorate the effects of tumor promoters on cell-cell communication. Additionally, adult stem cells are hypothesized to be the target cells for initiating the carcinogenic process. A new paradigm has been presented that postulates the first function of the carcinogenic process is to block the "mortalization" of a normal, "immortal" adult stem cell rather than the induction of "immortalization" of a normal mortal cell.

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Inhibitory effect of pentachlorophenol on gap junctional intercellular communication in rat liver epithelial cells in vitro

Cited by 6 publications

References 0 publications

Inhibition of gap-junctional intercellular communication and activation of mitogen-activated protein kinases by cyanobacterial extracts – Indications of novel tumor-promoting cyanotoxins?

Inhibition of gap-junctional intercellular communication and activation of mitogen-activated protein kinases by cyanobacterial extracts – Indications of novel tumor-promoting cyanotoxins?

Green tea: protective action against oxidative damage induced by xenobiotics

Dietary Modulation of the Multistage, Multimechanisms of Human Carcinogenesis: Effects on Initiated Stem Cells and Cell–Cell Communication

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